Negative cross‐resistance of a pyrethroid‐resistant Drosophila mutant to Phryma leptostachya ‐derived haedoxan A

拟除虫菊酯 氯菊酯 钠通道 生物 击倒阻力 黑腹果蝇 突变体 蟑螂 溴氰菊酯 联苯菊酯 毒理 遗传学 杀虫剂 化学 基因 生态学 有机化学 氟氯氰菊酯
作者
Xingtao Qie,Yuzhe Du,Ahmed A. A. Aioub,Ke Dong,Zhaonong Hu
出处
期刊:Insect Science [Wiley]
卷期号:29 (3): 817-826 被引量:1
标识
DOI:10.1111/1744-7917.12973
摘要

Voltage-gated sodium channels are the primary target of pyrethroid insecticides. Mutations in sodium channel confer knockdown resistance (kdr) to pyrethroids in various arthropod pests. Haedoxan A (HA) is the major insecticidal component from Phryma leptostachya. It has been shown that HA alters electrical responses at the Drosophila neuromuscular junction and modifies the gating properties of cockroach sodium channels expressed in Xenopus oocytes. However, whether sodium channel mutations that confer pyrethroid resistance also affect the action of HA is unknown. In this study, we conducted bioassays using HA and permethrin in two Drosophila melanogaster strains: w1118 , an insecticide-susceptible strain, and parats1 , a pyrethroid-resistant strain due to a I265N mutation in the sodium channel, and identified a new case of negative cross-resistance (NCR) between permethrin and HA. Both parats1 larvae and adults were more resistant to permethrin, as expected. However, both parats1 larvae and adults were more sensitive to HA compared to w1118 . We confirmed that the I265N mutation reduced the sensitivity to permethrin of a Drosophila sodium channel variant, DmNav 22, expressed in Xenopus oocytes. Interestingly, the I265N mutation also abolished the effect of HA on sodium channels. Further characterization showed that I265 on the sodium channels is critical for the action of both pyrethroids and HA on sodium channels, pointing to an overlapping mode of action between pyrethroids and HA on the sodium channel. Overall, our results suggest an I265N-independnt mechanism(s) in parats1 flies that is responsible for the NCR between permethrin and HA at the whole insect level.
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